Tsutsui Rika, Tsukagoshi Hiroyuki, Nagasawa Koo, Takahashi Masaki, Matsushima Yuki, Ryo Akihide, Kuroda Makoto, Takami Hideki, Kimura Hirokazu
Department of Pathologic Analysis, Division of Medical Life Sciences, Hirosaki University Graduate School of Health Sciences, 66-1, Hon-cho, Hirosaki-shi, Aomori 036-8564, Japan.
Aomori Prefecture Public Health and Environment Center, 1-1-1, Higashitsukurimichi, Aomori-shi, Aomori 030-8566, Japan.
J Med Microbiol. 2017 Feb;66(2):160-168. doi: 10.1099/jmm.0.000431.
To genetically explore the fusion protein gene (F) in human parainfluenza virus type 1 (HPIV1) and type 3 (HPIV3) strains, we analysed them in patients with acute respiratory infections in Eastern Japan from 2011 to 2015.
We constructed phylogenetic trees based on the HPIV and HPIV3 F gene using the maximum likelihood method and conducted P-distance and selective pressure analyses. We also predicted the linear epitopes of the protein in the prototype strains. Furthermore, we mapped the amino acid substitutions of the proteins.
Nineteen strains of HPIV1 and 53 strains of HPIV3 were detected among the clinical acute respiratory infection cases. The phylogenetic trees indicated that the HPIV1 and HPIV3 strains were classified into clusters II and III and cluster C, respectively. The P-distance values of the HPIV1 and HPIV3 F genes were <0.03. Two positive selection sites were inferred in the HPIV1 (aa 8 and aa 10), and one positive selection site was inferred in the HPIV3 (aa 108), but over 10 negative selection sites were inferred. Four epitopes were predicted for the HPIV1 prototype strains, while five epitopes were predicted for the HPIV3 prototype strain. A positive selection site (aa 108) or the HPIV3 F protein was involved in the predicted epitope. Additionally, we found that an amino acid substitution (R73K) in the LC76627 HPIV3 strain presumably may affect the resistance to neutralization by antibodies.
The F gene of HPIV1 and HPIV3 was relatively well conserved in the eastern part of Japan during the investigation period.
为了从基因层面探究1型人副流感病毒（HPIV1）和3型人副流感病毒（HPIV3）毒株中的融合蛋白基因（F），我们对2011年至2015年日本东部急性呼吸道感染患者中的这些毒株进行了分析。
我们使用最大似然法基于HPIV1和HPIV3的F基因构建了系统发育树，并进行了P距离和选择压力分析。我们还预测了原型毒株中该蛋白的线性表位。此外，我们绘制了该蛋白的氨基酸替换图谱。
在临床急性呼吸道感染病例中检测到19株HPIV1和53株HPIV3。系统发育树表明，HPIV1和HPIV3毒株分别被归类到II簇和III簇以及C簇。HPIV1和HPIV3的F基因的P距离值均<0.03。在HPIV1中推断出两个正选择位点（第8位氨基酸和第10位氨基酸），在HPIV3中推断出一个正选择位点（第108位氨基酸），但推断出超过10个负选择位点。预测HPIV1原型毒株有四个表位，而HPIV3原型毒株有五个表位。一个正选择位点（第108位氨基酸）或HPIV3 F蛋白参与了预测的表位。此外，我们发现LC76627 HPIV3毒株中的一个氨基酸替换（R73K）可能会影响对抗体中和作用的抗性。
在调查期间，HPIV1和HPIV3的F基因在日本东部相对保守。
